Signaling through TLR5 mitigates lethal radiation damage by neutrophil-dependent release of MMP-9.

ABSTRACT: Acute radiation syndrome (ARS) is a major cause of lethality following radiation disasters. A TLR5 agonist, entolimod, is among the most powerful experimental radiation countermeasures and shows efficacy in rodents and non-human primates as a prophylactic (radioprotection) and treatment (radiomitigation) modality. While the prophylactic activity of entolimod has been connected to the suppression of radiation-induced apoptosis, the mechanism by which entolimod functions as a radiomitigator remains poorly understood. Uncovering this mechanism has significant and broad-reaching implications for the clinical development and improvement of TLR5 agonists for use as an effective radiation countermeasure in scenarios of mass casualty resulting from accidental exposure to ionizing radiation. Here,

SUBMITTER: Brackett CM 

PROVIDER: S-EPMC8478872 | biostudies-literature | 2021 Sep

REPOSITORIES: biostudies-literature